Acrylamide and polyacrylamide are used in industry for the production of plastics. It has been supposed that the main exposure for acrylamide in the general population has been through drinking water and tobacco smoking Exposure via drinking water is small and the EU has determined maximum levels of 0.1 microgram per liter water.
Acrylamide is water soluble and is quickly absorbed in the digestive tract. Excretion via the urine is fast and half of acrylamide is cleared from the body in a few hours.
The toxicological effects of acrylamide are well known. It causes DNA damage and at high doses neurological and reproductive effects have been observed. Glycidamide, a metabolite of acrylamide, binds to DNA and can cause genetic damage. Prolonged exposure has induced tumours in rats, but cancer in man has not been convincingly shown. The International Agency for Research on Cancer (IARC) has classified acrylamide as a “probably carcinogenic to humans” (Group 2A).
Acrylamide has been shown to induce gene mutations in cultured animal cells and also in animals treated in vivo. Thus it is assumed that exposure also to very low doses of acrylamide increases the risk for mutation and cancer.
High doses of acrylamide have been applied in the toxicological studies, which is an accepted practice. 25-50 mg per kg body weight is the lowest dose that has been shown to increase the mutation frequency in mouse. Recent studies in the laboratory of the Swedish Food Administration have shown that chromosome aberrations are induced in mice at 10-20 times lower doses.
Among the acrylamide metabolites glycidamide is considered the most likely candidate for causing genetic damage. Glycidamide has been found in mice and rats, and also in humans exposed to acrylamide.
Neurological damage was observed when rats were given acrylamide in their drinking water. The lowest effective dose was 2 mg/kg body weight and day, and the highest no-effect dose was 0.5 mg/kg body weight and day. Also humans exposed to high doses of acrylamide have shown neurological damage, e.g. some workers occupied in the building of the tunnel at Hallandsåsen. It is difficult to assess the highest acrylamide dose in humans that does not cause neurological effects (NOEL). The level is probably several times higher than the average acrylamide intake from food.
Decreased fertility was observed in rats exposed to 5-10 mg acrylamide/kg body weight and day.
Epidemiological studies in man have not shown a correlation between exposure to acrylamide and increased cancer rate. These studies have been criticised because the number of studied persons was too low considering the expected effect.
Two long-term studies in rats have shown a substantial increase of tumours in different organs when the animals were exposed to acrylamide in drinking water. Similar studies have been made in mice. The lowest effective dose was 2 mg/kg body weight per day.
In the studies with rats the increase of tumours was most evident in specific organs, e.g. mammary gland, uterus, adrenal gland, scrotal mesothelium. In mice there was an increase of lung and skin tumours. These cancer studies have been used for the assessment of the risk of cancer in humans due to acrylamide exposure.
It should be noted that the genotoxic studies have indicated that there is no threshold value for the risk of cancer induced by acrylamide, i.e. there is no dose of acrylamide so low that it does not increase the risk of cancer. In making these assessments it is assumed that man and rat have the same sensitivity for cancer induction by acrylamide.
The results of the risk assessments are somewhat different since they are based on different mathematical models. By consumption of 1 microgram acrylamide/kg body weight per day the lifetime risk for cancer has been calculated to                4.5 per 1000 (U.S. EPA)        0.7 per 1000 (WHO)        10 per 1000 (Granath et al. 1999, Stockholm University)        
Recent analyses have now indicated that the exposure to acrylamide is probably considerably higher (for non-smokers) from consumption of certain foods that have been heated. As reported in J Agric Food Chem. 2002 Aug. 14; 50(17):4998-5006 a group at the University of Stockholm, headed by Prof. Margareta Tornqvist, has found that acrylamide is formed during heating of starch-rich foods to high temperatures.
The Swedish National Food Administration has developed a LC/MS/MS-method for the analysis of acrylamide in foods. Analysis has shown that acrylamide is present in a large number of foods, including many regarded as staple foods. The levels of acrylamide differ widely within each food group analysed.
Using information on the levels in different foods and Swedish food consumption data, it is suggested that a significant number of annual cancer cases can be attributed to acrylamide.
When foodstuffs were analysed at the Swedish National Food Administration (NFA) in Uppsala and at AnalyCen AB in Lidkoping it was found that some foodstuffs, which had been heated, could contain relatively high levels of the substance acrylamide. In total, more than 100 food samples have been analysed at the NFA. The food survey comprised bread, pasta, rice, fish, sausages, meat (beef and pork), biscuits, cookies, breakfast cereals and beer, etc as well as some ready-made dishes such as pizza and products based on potatoes, maize and flour.
The levels of acrylamide vary considerably between single foodstuffs within food groups, but potato crisps and French fries generally contained high levels compared to many other food groups. The average content in potato crisps is approximately 1000 microgram/kg and in French fries approximately 500 microgram/kg. Other food groups which may contain low as well as high levels of acrylamide are crisp bread, breakfast cereals, fried potato products, biscuits, cookies and snacks, e.g. popcorn.
Foodstuffs which are not fried, deep fried or oven-baked during production or preparation are not considered to contain any appreciable levels of acrylamide. No levels could be detected in any of the raw foodstuffs or foods cooked by boiling investigated so far (potato, rice, pasta, flour and bacon).
According to the NFA food survey “Riksmaten 1997-98”, which is based on approximately 1200 individuals between the age of 17 to 70 who recorded their food consumption during one week, an average intake of acrylamide of approximately 25 microgram per day (maximum intake is approximately six times higher) is obtained, based on the food groups shown below. The remaining food groups are estimated to account for approximately 10-15 microgram of acrylamide; in total an average intake of 35-40 microgram. The percentage contribution based on an intake of 40 microgram acrylamide per day results in:                potato products: 36% (French fries 16%, fried potatoes 10%, crisps 10%)        bread: 16%        biscuits, cookies and wafers: 5%        breakfast cereals: 3%        remaining foodstuffs groups, basically not investigated yet: 40%        
Young adults (17 to 34 years of age) have, according to “Riksmaten”, a higher consumption of snacks (nuts, chips and popcorn) than other adults. For children under 17 years of age newer data are lacking In the food survey “Ungdom mot år 2000” (Samuelson et al 1996), which was carried out 1993-94 among 15-year olds in Uppsala and Trollhättan, the consumption of snacks was comparable to that of young adults in Riksmaten. Children have a lower average body weight than the 70 kg generally assumed when carrying out risk assessments. This implies that the food intake per kg body weight and the exposure to various substances could be even larger for those groups of individuals compared to adults. According to Riksmaten, 10 percent of the adult population consumes 90 percent of the snacks consumed in Sweden.
An alternative way of estimating the intake of acrylamide is by adduct measurement, that is to measure a reaction product of acrylamide with the protein of the blood, the haemoglobin (Tornqvist et al 1997). This reaction product seems to occur in all investigated humans at approximately the same levels and is furthermore a measurement of the continuously administered dose of acrylamide. The reason is unknown in this case, but workers who were exposed to acrylamide at the tunnel accident at Hallandsåsen in Sweden had higher levels of this reaction product in their blood.
In the general population, although not in smokers (who have a level of this adduct 2-3 times the background level), the background level has been estimated to account for a daily intake corresponding to approximately 100 microgram per day.
Other sources than foodstuffs (estimated average intake of 35-40 μg/day), e.g. cosmetics, drinking water, and a possible endogenous formation in the body of acrylamide, could, to a lower extent contribute to the background level. Estimated administered amount of acrylamide for the formation of the background level together with levels of acrylamide in foodstuffs are, however, presently extremely uncertain.
A Report from Swedish Scientific Expert Committee entitled “Acrylamide In Food-Mechanisms of formation and influencing factors during heating of foods” discloses possible mechanisms for the formation of acrylamide in food. Relevant extracts from this report are given below in Appendix 1.
According to Health Canada, model experiments carried out in the Food Directorate showed that when asparagine is heated with glucose, acrylamide is produced. In an open letter, Health Canada stated “The production of acrylamide in these studies was temperature dependent and gave comparable results to those found when potato slices were similarly heated. At this time, not much is known about other possible pathways of formation of acrylamide in foods.”
Further discussion of reactions occurring during heating of food is given in Principles of Food Chemistry pages 100-109. This discussion is provided in Appendix 2.
The present invention alleviates the problems of the prior art.
Some aspects of the invention are defined in the appended claims.